concanavalin-a and Poultry-Diseases

This article describes the in vitro and in vivo effects of a 25-hydroxycholecalciferol (25[OH]D) treatment in layer hens during a mixed coccidia challenge. HD11 cells (chicken macrophage cell line) were treated in vitro with a coccidia antigen or in a medium supplemented with either 1,25-dihydroxycholecalciferol (1,25[OH]2D) or 25(OH)D. HD11 cells treated in vitro with 200 nM of 1,25(OH)2D had increased nitrite production (P < 0.01) compared with HD11 cells treated with 0 or 200 nM of 25(OH)D. Treating HD11 cells with 25(OH)D decreased IL-10 mRNA by 1.7-fold, but 1,25(OH)2D treatment increased the amount of IL-10 mRNA by 2.7-fold (P < 0.01) compared with the group treated with 0 nM of 25(OH)D. Post-coccidial antigen stimulation, 25(OH)D or 1,25(OH)2D treatment decreased (P < 0.01) 1α-hydroxylase mRNA amounts in HD11 cells. Stimulating primary T cells in vitro with Concanavalin A (Con-A) decreased (P = 0.020) the 1α-hydroxylase mRNA amounts by 3-fold. ConA-B1-VICK cells (chicken T cell line) stimulated with 100 nM 1,25(OH)2D or with supernatants from HD11 cells treated with 25(OH)D plus lipopolysaccharide (LPS) had 1.3-fold less (P < 0.01) interferon (IFN)-γ mRNA compared with the group treated with 25(OH)D. Layer birds were fed a basal diet supplemented with 25(OH)D at 6.25, 25, 50, or 100 μg/kg, and at 21 d of age orally challenged with 1 × 10(5) live coccidia oocysts. Compared with birds fed similar levels of 25(OH)D and unchallenged with the coccidia oocyst, birds challenged with the coccidia oocyst had 15% reduced BW gain in the groups supplemented with either 6.25, 25, or 50 μg/kg of 25(OH)D, but only a 4% reduced BW gain in birds fed 100 μg/kg of 25(OH)D (P < 0.01). Birds fed 100 μg/kg 25(OH)D had decreased (P = 0.012) CD8+ cell percentages in cecal tonsils in both coccidial oocyst challenged and unchallenged birds, compared with birds fed 6.25 μg/kg 25(OH) and unchallenged with coccidial oocysts. At 15 d post-coccidia challenge, birds fed 100 μg/kg 25(OH)D and challenged with coccidial oocysts had 17% more CD4+CD25+ cells (P = 0.018) in the cecal tonsil compared with the birds fed 100 μg/kg 25(OH)D and unchallenged with coccidial oocysts. At d 6 post-coccidia challenge, birds fed 100 μg/kg 25(OH)D had a 3.5-fold increase (P < 0.01) in IL-10 mRNA amounts in the cecal tonsils compared with birds fed 6.25 μg/kg 25(OH)D. In conclusion, supplementing birds with 100 μg/kg 25(OH)D could be a nutritional strategy to reduce the production losses post-coccid

Topics: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; Animals; CD8-Positive T-Lymphocytes; Cecum; Cell Line; Chickens; Coccidiosis; Concanavalin A; Dietary Supplements; Dose-Response Relationship, Drug; Female; Interleukin-10; Lipopolysaccharides; Macrophages; Poultry Diseases; Vitamin D

The ban on the use of antibiotics as feed additives for animal growth promotion in the European Union and United States and the expectation of this trend to further expand to other countries in the short term have prompted a surge in probiotic research. Multi-species probiotics including safe and compatible strains with the ability to bind different nutritional lectins with detrimental effects on poultry nutrition could replace antibiotics as feed additives.

Topics: Animals; Anti-Infective Agents; Antibiosis; Bifidobacterium longum subspecies infantis; Cell Line; Cell Survival; Concanavalin A; Drug Resistance, Bacterial; Enterococcus faecium; Epithelial Cells; Lactobacillus; Lectins; Models, Theoretical; Plant Lectins; Poultry Diseases; Probiotics; Propionibacterium; Protein Binding; Soybean Proteins; Virulence; Virulence Factors; Wheat Germ Agglutinins

The effects of dietary supplementation with an organic extract of Curcuma longa on systemic and local immune responses to experimental Eimeria maxima and Eimeria tenella infections were evaluated in commercial broiler chickens. Dietary supplementation with C. longa enhanced coccidiosis resistance as demonstrated by increased BW gains, reduced fecal oocyst shedding, and decreased gut lesions compared with infected birds fed a nonsupplemented control diet. The chickens fed C. longa-supplemented diet showed enhanced systemic humoral immunity, as assessed by greater levels of serum antibodies to an Eimeria microneme protein, MIC2, and enhanced cellular immunity, as measured by concanavalin A-induced spleen cell proliferation, compared with controls. At the intestinal level, genome-wide gene expression profiling by microarray hybridization identified 601 differentially expressed transcripts (287 upregulated, 314 downregulated) in gut lymphocytes of C. longa-fed chickens compared with nonsupplemented controls. Based on the known functions of the corresponding mammalian genes, the C. longa-induced intestinal transcriptome was mostly associated with genes mediating anti-inflammatory effects. Taken together, these results suggest that dietary C. longa could be used to attenuate Eimeria-induced, inflammation-mediated gut damage in commercial poultry production.

Topics: Animal Feed; Animals; Antibodies, Protozoan; Cell Proliferation; Chickens; Coccidiosis; Concanavalin A; Curcuma; Diet; Dietary Supplements; Eimeria; Feces; Gene Expression Regulation; Immunity, Cellular; Immunity, Humoral; Intestinal Mucosa; Lymphocytes; Oligonucleotide Array Sequence Analysis; Parasite Egg Count; Plant Extracts; Poultry Diseases; Protozoan Proteins; Reverse Transcriptase Polymerase Chain Reaction; Spleen

Concanavalin A-Sandwich ELISA (Con A-S-ELISA) was developed for the detection of infectious bronchitis virus (IBV) or chicken specific anti-viral antibodies. The antigen detection limit for the Con A-S-ELISA was 10(5,1) EID(50)/mL. Three homologous and four heterologous IBV strains were similarly detected. This assay was highly effective in detecting the virus after infected tissue homogenates were passed once in embryonated chicken eggs, showing a good agreement with virus isolation technique. The Con A-S-ELISA was also used to measure anti-IBV chicken antibodies and showed a high coefficient of correlation (r = 0.85) and an agreement of k = 0.80 with the commercially available Indirect-ELISA. The relative sensitivity and specificity between these two tests were, respectively, 92.86% and 95.65% with an accuracy of 93.39%. Thus, the Con A-S-ELISA proved to be able to detect alternatively homologous and heterologous IBV strains or specific chicken anti- IBV antibodies, using the Con A as capture reagent of this assay.

Topics: Animals; Antibodies, Viral; Antibody Specificity; Chickens; Concanavalin A; Coronavirus Infections; Enzyme-Linked Immunosorbent Assay; Infectious bronchitis virus; Poultry Diseases; Reproducibility of Results; Sensitivity and Specificity

Studies were performed to determine the effects of Bcell suppression on the pathogenesis of Subgroup J avian leukosis virus (ALV-J) in broiler chickens. Neonatal chickens were treated with cyclophosphamide (CY) or PBS, and then infected with ALV-J (ADOL-7501) at 2 weeks of age. CY treatment induced B cell specific immunosuppression throughout the experiment confirmed by decreased bursal weight, intact lymphocyte mitogenetic activity stimulated by Con A and increased relative subpopulation of CD3-positive cells as measured by flow cytometry. Chickens in this experiment had Mareks disease virus exposure prior to three weeks of age as determined by the presence of lymphocytic infiltration and antibody. Virus neutralizing antibody against ALV-J was first observed at 6 weeks post-infection in some of the infected chickens in the PBS group. As expected, none of the chickens from the CY group and uninfected chickens developed virus-neutralizing antibody. The viremic status was measured by real time RT-PCR using SYBR green I dye. The percentage of viremic chickens was significantly higher, and more chickens had high titered viremia, in the CY treated group. No neoplastic foci consistent with ALVJ infection were observed in any of the experimental chickens. The frequency and intensity of viral antigen expression determined by immunohistochemistry was significantly higher in tissues from CY treated birds than those of PBS treated chickens at 3 weeks post-infection. This study showed that B cell specific immunosuppression with CY treatment in chickens resulted in increase in viremia and viral antigen load in tissues.

Topics: Animals; Avian Leukosis; Avian Leukosis Virus; Benzothiazoles; Body Weight; Bursa of Fabricius; Chickens; Concanavalin A; Cyclophosphamide; Diamines; Flow Cytometry; Immunocompromised Host; Immunohistochemistry; Immunophenotyping; Immunosuppressive Agents; Lymphocyte Activation; Organic Chemicals; Poultry Diseases; Quinolines; Random Allocation; Reverse Transcriptase Polymerase Chain Reaction; RNA, Viral; Spleen; Statistics, Nonparametric; Viremia

Effects of different durations of cold stress (CS) and the time point of immunization relative to the CS of 3 chicken lines were studied. The first 2 chicken lines were divergently selected for high and low antibody responses, and the third was a random-bred control line. In 2 experiments, 26-d-old growing chicks of the 3 lines were feed restricted at 80% of ad libitum and subjected to CS of 10 degrees C for 7, 2, or 0 d. Birds were immunized with keyhole limpet hemocyanin (KLH) at -1, +1, +3, +5, or +7 d relative to the end of the CS treatment. Specific antibodies to KLH were determined. In addition, in vitro lymphocyte proliferation responses to concanavalin A (ConA) and KLH as measures of cell-mediated immunity, production of zymosan-induced reactive oxygen intermediates as a measure of phagocytosis, and BW gain as a measure of a production trait were determined. Significantly higher antibody responses to KLH were found in the high line as compared with the other 2 lines. Specific antibody responses to KLH were not significantly affected by the CS treatments. CS had a delayed effect on in vitro mitogen responses to ConA. In vitro lymphocyte proliferation responses to ConA were higher in the low line birds than in the other 2 lines. In general, 7 d of CS significantly enhanced cellular immunity to ConA in vitro, whereas the 2-d CS treatment had differential effects on lymphocyte proliferation to ConA, depending on the line of bird and the time of immunization. KLH-specific lymphocyte proliferation was enhanced by 2 d of CS at 28 d after immunization. Effects of various CS treatments and the time of immunization on the production of reactive oxygen intermediates were inconsistent. In addition, BW gain was negatively affected by CS. We concluded that the innate part of the immune system (phagocytes) responded immediately to CS with an as yet unexplained variability, irrespective of the genetic background. When CS was prolonged, the cellular adaptive immune response and, to some extent, the specific humoral immune response were also affected. The lack of line-by-treatment interactions suggested that the genetic background was a prominent factor for the magnitude of the specific immune response. Our data confirmed earlier studies that, under restricted feeding with simultaneous stress (energy demand for thermoregulation and growth), cellular immunity is more sensitive than humoral immunity. A negative correlation between BW gain and cellular immunity sugges

Topics: Animals; Antibodies; Antibody Formation; Chickens; Cold Temperature; Concanavalin A; Hemocyanins; Immunity, Cellular; Immunization; Lymphocyte Activation; Poultry Diseases; Reactive Oxygen Species; Selection, Genetic; Stress, Physiological; Weight Gain

Our previous work showed that the cell-mediated immunity (CMI) was enhanced by live Salmonella vaccine (LV). The objective of this study was to evaluate the impact of live and killed Salmonella vaccines on Salmonella enteritidis (SE) clearance and to determine if the clearance was mediated by cell-mediated and/or humoral immunity. Chickens were first immunized at 2 weeks of age followed by a booster dose at 4 weeks, challenged with live SE 2 weeks later (6-week-old) and tested for CMI, antibody response and SE clearance 1-week post SE-challenge (7-week-old). Spleen cell proliferation induced by SE-flagella and Concanavalin A (Con A) were significantly higher and SE shedding was significantly lower in the LV group. The splenic CD3 population was significantly lower and B cells were higher in the control group compared to all the SE-challenged groups (with and without vaccination). Serum antibody to SE-flagella and envelope were significantly higher in the KV group compared to all the other groups. These results suggest that LV protects against SE infection, probably by enhancing the CMI.

Topics: Animals; Antibodies, Bacterial; Cell Division; Chickens; Concanavalin A; Feces; Flagella; Flow Cytometry; Poultry Diseases; Salmonella enteritidis; Salmonella Infections, Animal; Salmonella Vaccines; Specific Pathogen-Free Organisms; Spleen; Statistics, Nonparametric; Vaccines, Attenuated; Vaccines, Inactivated

The role of cell-mediated immunity (CMI) in pathogenesis of infectious bursal disease virus (IBDV) was investigated. One-day-old specific pathogen-free chickens were treated with 3mg of cyclophosphamide (Cy) per chicken for 4 consecutive days and, 3 weeks later, infected with the IBDV-IM strain. Chickens were examined for: (a) mitogenic response of splenocytes to ConA, as an indicator of T-cell functions in vitro, (b) antibody against IBDV by ELISA, (c) IBDV genome in various tissues by RT-PCR and (d) immunological memory. At the time of IBDV infection, Cy-treated chickens had depleted bursal tissue (an avian primary B-cell lymphoid organ), severely compromised antibody-producing ability, but normal T-cell response to ConA. In primary infection, no detectable antibody against IBDV antigen in Cy-treated, IBDV-infected chickens was observed up to 28 days post-infection (PI), while IBDV genome was detected by RT-PCR in spleen, thymus, liver and blood until 10 days PI. Like intact control chickens infected with IBDV, Cy-treated, IBDV-infected chickens suppressed splenocytes responses to ConA from 5 to 10 days PI, suggesting that intact control as well as Cy-treated chickens responded similarly to IBDV infection in the early phase. Following re-infection with IBDV, no detectable secondary antibody response to IBDV as well as IBDV genome in tissues were observed in Cy-treated chickens, while intact control chickens developed vigorous secondary antibody response. Similar to intact control chickens infected with IBDV, Cy-treated chickens after second infection with IBDV did not suppress splenocyte response to ConA. These results suggested that in the absence of detectable anti-IBDV antibodies, protection of Cy-treated chickens from IBDV infection may occur via immunological memory mediated by CMI. We concluded that under normal conditions, IBDV induces a protective antibody response, however, in the absence of antibody, CMI alone is adequate in protecting birds against virulent IBDV.

Topics: Animals; Antibodies, Viral; Antibody Specificity; B-Lymphocytes; Birnaviridae Infections; Chickens; Concanavalin A; Cyclophosphamide; Enzyme-Linked Immunosorbent Assay; Immunosuppressive Agents; Infectious bursal disease virus; Poultry Diseases; Reverse Transcriptase Polymerase Chain Reaction; Specific Pathogen-Free Organisms; Spleen; T-Lymphocytes; Time Factors

The effects of vitamin A (VitA) deficiency on the host intestinal immune response and disease susceptibility to coccidiosis were investigated in broiler chickens following oral infection with Eimeria acervulina (EA). Day-old male broilers were fed milo-soybean meal diets either with 8,000 IU VitA/kg feed (CONT) or without added VitA (A-DEF). At 25 d, a group of randomly selected birds from each treatment was inoculated orally with EA-sporulated oocysts. Intestinal immune response was assessed by the changes in the duodenum intraepithelial lymphocyte (IEL) subpopulations using flow cytometry at 35 d in in fected and noninfected birds. Concanavalin A (ConA)-induced spleen lymphocyte proliferation was tested using dimethylthiazol diphenyltetrazolium bromide colorimetric assay. Whether challenged or not with EA, A-DEF birds had fewer IEL expressing the surface markers CD3, CD4, CD8, alphabetaTCR, and gammabetaTCR. Without EA challenge, A-DEF birds had more surface IgA-expressing cells than CONT birds. Upon challenge, A-DEF chickens showed lower CD4+ IEL than CONT chickens. Following EA infection, CD8+ IEL increased in the CONT group, whereas no change was found in CD8+ IEL of A-DEF birds. A higher number of EA oocysts was recovered from A-DEF birds than from CONT birds (9.2 x 10(8) vs 5.4 x 10(8), respectively; P < or = 0.05). Serum samples taken 10 d post challenge showed higher antibody level against a recombinant coccidial antigen in A-DEF birds than in CONT birds. The A-DEF birds showed depressed ConA-induced lymphoproliferation response and produced lower serum interferon-gamma than CONT birds. These data show that VitA deficiency compromised local immune defenses of challenged birds, as reflected in lymphocyte profiles, oocyst shedding, and interferon-gamma levels in A-DEF birds.

Topics: Animals; Antibodies, Protozoan; CD3 Complex; CD4 Antigens; CD8 Antigens; Chickens; Coccidiosis; Colorimetry; Concanavalin A; Duodenum; Eimeria; Epithelium; Flow Cytometry; Interferon-gamma; Lymphocyte Activation; Lymphocyte Count; Lymphocytes; Poultry Diseases; Spleen; Vitamin A Deficiency

Interleukin (IL)-2 is a major cytokine of cell-mediated immunity (CMI). Because chickens infected with Eimeria, the causative agent of coccidiosis, develop a robust cell-mediated response against the parasite, we measured IL-2 concentrations in vivo and in vitro during the course of primary and secondary experimental Eimeria tenella infections. IL-2 levels in serum and culture supernatants of spleen lymphocytes stimulated with mitogen or E. tenella sporozoites were significantly increased on day 7 post-primary infection compared with control group. This peak in IL-2 coincided with the time of maximum intestinal lesions as measured by cecum lesion scores. By contrast, during secondary infection highest IL-2 concentrations preceded intestinal lesions by 5 days (day 2 versus day 7, respectively). These results confirmed that IL-2 production is augmented during experimental coccidiosis and suggested that cellular immunity elicited during an anamnestic response to parasite reinfection is mediated, at least in part, by IL-2.

Topics: Animals; Cecum; Cells, Cultured; Chickens; Coccidiosis; Concanavalin A; Disease Models, Animal; Eimeria tenella; Interleukin-2; Intestines; Kinetics; Poultry Diseases; Spleen; Sporozoites

Continuous culture of concanavalin A (Con A)-activated spleen cells in the presence of chicken recombinant IL-2 (rIL-2) promoted preferential growth of gammadelta T-cells. These cells displayed a high level of spontaneous cytotoxicity against LSCC-RP9 tumor cells, an avian NK cell target. Stimulation of IL-2-dependent gammadelta T-cells with Con A induced IFN-gamma and IL-2 mRNA transcripts, whereas stimulation with rIL-2 induced only IFN-gamma mRNA. Subcutaneous injection of 3-week-old chickens with IL-2 DNA increased splenic cells, expressing the CD8 and gammadelta TCR antigens. To investigate the role of IL-2 and gammadelta T-cells in parasitic infection, chickens were orally infected with Eimeria acervulina and the expression of IL-2 mRNA transcripts in the spleen and duodenum and the percentage of gammadelta T-cells in the duodenum were examined. Following both, the primary and secondary infections, a significant enhancement of IL-2 mRNA transcripts in the spleen and intestine and increased percentage of intraepithelial gammadelta T-cells in the duodenum were observed. These results indicate that host immune responses to E. acervulina involve an up-regulation of IL-2 secretion and an increased duodenum gammadelta T-cells.

Topics: Animals; Chickens; Coccidiosis; Concanavalin A; Cytotoxicity, Immunologic; DNA Primers; Duodenum; Eimeria; Flow Cytometry; Interferon-gamma; Interleukin-2; Killer Cells, Natural; Lymphocyte Activation; Polymerase Chain Reaction; Poultry Diseases; Receptors, Antigen, T-Cell, gamma-delta; Recombinant Proteins; RNA, Messenger; Spleen; T-Lymphocytes; Up-Regulation

We examined the suppressive activity of bursal T cells induced by infectious bursal disease virus (IBDV) in inbred (15x7) and outbred commercial specific-pathogen-free (SPF) chickens. The suppressive activity was measured by the ability of bursal and splenic T cells from IBDV-infected chickens to inhibit mitogenic responses of normal splenocytes. The bursacytes but not the splenocytes of IBDV-infected chickens inhibited the mitogenic responses of normal splenocytes. The mitogenic inhibition by the bursacytes of IBDV-infected chickens was dose-dependent. The suppression was observed both in inbred and non-inbred chickens, and thus, was non MHC-restricted. Cell-sorting experiments revealed that both CD4(+) and CD8(+) cells from the bursa of IBDV-infected chickens, as well as cell-culture supernatants conditioned by these cells, mediated suppression. Suppressor T (Ts) cells may therefore be involved in the immunosuppression induced by IBDV.

Topics: Animals; Birnaviridae Infections; Bursa of Fabricius; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Chick Embryo; Chickens; Concanavalin A; Flow Cytometry; Infectious bursal disease virus; Lymphocyte Activation; Poultry Diseases; Random Allocation; Scintillation Counting; Specific Pathogen-Free Organisms; Spleen

We examined the effects of infectious bursal disease virus (IBDV) on splenic T cells and macrophages. In acute IBDV infection, splenocytes responded poorly to Con A stimulation. However, when T cells were isolated from whole spleen cells, purified T cells responded normally to Con A. This result indicated that functional T cells were present in the spleen but mitogen-induced proliferation of T cells was being suppressed by other cells. Previous studies indicated that soluble factors from suppressor cells may mediate this inhibition of T cell mitogenesis. We thus examined the effects of IBDV on spleen adherent cells. Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to quantitate the expression of several cytokine genes in splenic macrophages. In acute IBDV infection, splenic macrophages exhibited enhanced gene expression of type I interferon (IFN), chicken myelomonocytic growth factor (cMGF), an avian homolog of mammalian IL-6, and 9E3/CEF4, an avian homolog of mammalian IL-8. Mitogen-stimulated spleen cell cultures also produced elevated levels of nitric oxide. The elevation of cytokine gene expression by macrophages occurred transiently during the acute phase of viral infection and coincided with in vitro inhibition of T cell mitogenic response of spleen cells.

Topics: Acute Disease; Animals; Avian Proteins; Base Sequence; Birnaviridae Infections; Chickens; Concanavalin A; Cytokines; DNA Primers; Gene Expression; Growth Substances; In Vitro Techniques; Infectious bursal disease virus; Intercellular Signaling Peptides and Proteins; Interferon Type I; Lymphocyte Activation; Macrophages; Nitric Oxide; Polymerase Chain Reaction; Poultry Diseases; Spleen; T-Lymphocytes

We have previously shown that the proportion of CD8-expressing T cells (CD8bright+ and CD4+ CD8dim+ cells) in the peripheral blood of chickens increases around 8 days after a primary infection with Eimeria tenella oocysts. The increase in the CD8+ eight cells coincides with enhanced responses after in vitro stimulation with parasite antigen. In the study described here, the responsiveness of these day 8 PBL was further characterized by determining their capacity to proliferate and to produce cytokine (IFN-gamma) upon stimulation with E. tenella sporozoite antigen, or non-specific stimuli like T cell growth factor (TCGF) and anti-CD3 monoclonal antibody (MoAb). Comparing the responsiveness of infected responder (day 8) and control chickens, non-specific triggering induced cytokine production in cells from infected animals and proliferation in cells from control animals. When triggered with E. tenella sporozoite antigen, lymphocytes from infected chickens responded with proliferation and cytokine production, in contrast to lymphocytes from control animals that did not respond. The phenotype of the lymphocytes involved in the parasite-specific proliferation and cytokine production, was characterized in a blocking assay using MoAb directed against the CD4 or CD8 molecule. The results suggest that CD8bright+ as well as CD4+ (CD4+ CD8dim+ and possible CD4+, single positive) lymphocytes are responsible for the IFN-gamma production measured after stimulation with parasite antigen, whereas the specific proliferative response appears to be caused by CD4+ (CD4+ CD8dim+ and possibly CD4+ single positive) lymphocytes. We speculate that the CD8bright+ cells, present in the circulation around 8 days after a primary E. tenella infection, act as effector cells in protective immune responses, whereas CD4+ cells play an important helper function in these responses.

Topics: Animals; Antigens, Protozoan; CD3 Complex; Cells, Cultured; Chickens; Coccidiosis; Concanavalin A; Eimeria tenella; Interleukin-2; Lymphocytes; Mitogens; Phenotype; Poultry Diseases; T-Lymphocytes

The response of lymphocytes to concanavalin A (Con A) was examined in the functionally hypothyroid SLD strain and the normal K strain chickens which were fed diets with or without T3 supplementation (0.1, 0.5 and 1.0 ppm) since the time of hatch. Peripheral blood lymphocytes (PBL) from 3 and 12 week old male and female chickens were incubated with Con A for 60 h. Mitogenic responsiveness was assessed by measuring the uptake of 3H-thymidine during the last 24 h of incubation. There was no difference in the mitogen response between male and female chickens. The mitogen responsiveness of PBL from the K strain tended to be greater than that from the SLD strain at both ages. The lowest dose of T3 (0.1 ppm) had no effect on the mitogen response of 3-week-old K strain chicks but caused an increase in mitogen response in 3-week-old SLD and in 12-week-old birds of both strains. Supplementation with 0.5 and 1.0 ppm T3 tended to decrease mitogen responsiveness in the K and SLD strain at both ages. The effect of treatment on thymus weights, bursa weights, and lymphocyte concentrations of the blood was also assessed.

Topics: Animals; Body Weight; Chickens; Concanavalin A; Female; Hypothyroidism; Leukocyte Count; Lymphocyte Activation; Lymphoid Tissue; Male; Organ Size; Poultry Diseases; Sex Factors; T-Lymphocytes; Triiodothyronine

Sequential study of permeability and cellular responses following intradermal concanavalin A in the chicken skin, using the colloidal carbon technique, revealed an increase in vascular permeability which was mostly confined to venules. A noteworthy feature of the reaction was marked accumulation of basophils, even in the later stages, and the early appearance of perivascular lymphoid aggregations. The occurrence of well formed giant cells, hypertrophy and hyperplasia of vascular endothelium and marked acanthosis of the epidermis were the other prominent changes. The findings suggest that Con A, in the chicken, appears to have a more general effect on the different types of cells and that it may act as a mitogen not only for T lymphocytes but also for endothelial and epithelial cells.

Topics: Animals; Basophils; Capillary Permeability; Chickens; Concanavalin A; Endothelium; Female; Hyperplasia; Injections, Intradermal; Leukocytes; Male; Necrosis; Poultry Diseases; Skin; Time Factors; Venules